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Links from GEO DataSets

Items: 20

1.

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [human]

(Submitter supplied) To explore the primary cause of Dilated Cardiomyopathy in heart samples from DCM-diagnosed patients who had undergone heart transplant (hDCM), we set out to identify differentially expressed genes by massively parallel sequencing of heart samples.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
10 Samples
Download data: XLS
2.

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL10999 GPL11002
16 Samples
Download data
Series
Accession:
GSE65447
ID:
200065447
3.

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cardiac-specific Bmi1 deletion [mouse]

(Submitter supplied) To explore the primary cause of Dilated Cardiomyopathy in Bmi1-null mice, we set out to identify differentially expressed genes by massively parallel sequencing of heart samples from Bmi1f/f;αMHCTM-Cretg/+ mice versus αMHCTM-Cretg/+ control mice (17 weeks postinduction).
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
6 Samples
Download data: TXT
Series
Accession:
GSE64391
ID:
200064391
4.

Bmi1 defines long-term adult cardiac stem cells in heart homeostasis and repair

(Submitter supplied) We have found the existence of a Bmi1+ population in the adult heart contributing to the organ low-rate turnover and repair with the generation of new cardiomyocytes. We show that the Bmi1+ population is a sub-population of the cardiac Sca-1+ progenitor cells. We have analyzed the gene profile by deep-sequencing (RNA-Seq) of Bmi1+ and Sca-1+Bmi1- cells in homeostatic heart condition. On the other hand, we have compared gene profile by deep-sequencing (RNA-Seq) of Bmi1+ cells in homeostatic condition versus Bmi1+ cells 5 days after myocardial infarction (MI). more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11002
12 Samples
Download data: XLS
Series
Accession:
GSE55754
ID:
200055754
5.

Distinct effects of genetic and pharmacological inhibition of galectin-3 on cardiac fibrosis and function in a mouse model of dilated cardiomyopathy

(Submitter supplied) Background: Galectin-3 is upregulated in heart disease, and its inhibition has been reported to confer benefits on cardiac remodeling and dysfunction. It remains unknown whether galectin-3 plays a biological role in a setting of dilated cardiomyopathy (DCM). We determined galectin-3 expression in transgenic (TG) mice with cardiac-restricted overexpression of mammalian sterile 20-like kinase 1 (Mst1-TG), and studied the effects of pharmacological and genetic inhibition of galectin-3 on the DCM phenotype. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
26 Samples
Download data: TSV
Series
Accession:
GSE106201
ID:
200106201
6.

Med1 Deletion in Heart Causes Dilated Cardiomyopathy

(Submitter supplied) Global gene expression analysis reveals that Med1 regulates many genes involved in energy metabolism, calcium signaling, and oxidative phosphorylation in myocardium.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
2 Samples
Download data: TXT
Series
Accession:
GSE65873
ID:
200065873
7.

RNA-seq analysis of human heart failure

(Submitter supplied) The goal of this study is to compare the transcriptome of heart failure patients (with ischemic or dilated cardiomyopathy) undergoing heart transplantation compared with healthy controls.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16288
36 Samples
Download data: TXT
8.

RNA-seq of heart failure in human left ventricles

(Submitter supplied) The goal of this dataset was to use RNA-seq in human heart tissue to delineate etiology-specific gene expression signatures in heart failure.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
64 Samples
Download data: TXT
9.

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

(Submitter supplied) Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy primarily of the right ventricle characterized through fibrofatty replacement of cardiomyocytes. The genetic etiology in ARVC patients is most commonly caused by dominant inheritance and high genetic heterogeneity. Though histological examinations of ARVC affected human myocardium reveals fibrolipomatous replacement, the molecular mechanisms leading to loss of cardiomyocytes are largely unknown. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
38 Samples
Download data: CEL
Series
Accession:
GSE29819
ID:
200029819
10.

Transcriptional effects of CTGF inhibition in a transgenic mouse model of dilated cardiomyopathy

(Submitter supplied) Cardiac structural changes associated with dilated cardiomyopathy (DCM) include cardiomyocyte hypertrophy and myocardial fibrosis. Connective Tissue Growth Factor (CTGF) has been associated with tissue remodeling and is highly expressed in failing hearts. To test if inhibition of CTGF would alter the course of cardiac remodeling and preserve cardiac function in the protein kinase Cε (PKCε) mouse model of DCM. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
44 Samples
Download data: CEL
Series
Accession:
GSE68857
ID:
200068857
11.

Loss of Cardiac microRNA-Mediated Regulation Leads to Dilated Cardiomyopathy and Heart Failure.

(Submitter supplied) RATIONALE: Heart failure is a deadly and devastating disease that places immense costs on an aging society. To develop therapies aimed at rescuing the failing heart, it is important to understand the molecular mechanisms underlying cardiomyocyte structure and function. OBJECTIVE: microRNAs are important regulators of gene expression, and we sought to define the global contributions made by microRNAs toward maintaining cardiomyocyte integrity. more...
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL9250
2 Samples
Download data
Series
Accession:
GSE32881
ID:
200032881
12.

Targeting MRTF/SRF in CAP2-dependent dilated cardiomyopathy delays disease onset

(Submitter supplied) About one third of dilated cardiomyopathy (DCM) cases are caused by mutations in sarcomere or cytoskeletal proteins. Yet treating the cytoskeleton directly is not possible because drugs that bind to actin are not well tolerated. Mutations in the actin binding protein CAP2 can cause DCM and knockout mice, either whole body (CAP2 KO) or cardiomyocyte specific knockouts (CAP2 CKO), develop DCM with cardiac conduction disease. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL21103 GPL18635
16 Samples
Download data: TXT
Series
Accession:
GSE125603
ID:
200125603
13.

BMI1 stress-related functions contribute to the redox-dependent fate of adult cardiac progenitors

(Submitter supplied) The accumulation of reactive oxygen species (ROS) is linked to several cardiovascular pathologies; it is also associated with cell cycle exit by nenonatal cardiomyocytes, a key limiting factor in the regenerative capacity of the adult mammalian heart. BMI1 is a component of the polycomb complex 1, which is linked to adult multipotent progenitors, and is also an important partner in DNA repair and redox regulation. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: BED
Series
Accession:
GSE92700
ID:
200092700
14.

Integrated Omic Analysis of a Guinea Pig Model of Heart Failure and Sudden Cardiac Death

(Submitter supplied) Sudden cardiac death (SCD) associated with heart failure (HF) is a multifactorial problem requiring a systems level approach applied to suitable experimental animal models with features of the human disease. Here we examine key regulatory pathways underlying the transition from compensated hypertrophy (HYP) to decompensated HF and SCD by integrated analysis of the transcriptome, proteome and metabolome. more...
Organism:
Cavia porcellus
Type:
Expression profiling by array
Platform:
GPL21468
18 Samples
Download data: CEL
Series
Accession:
GSE78077
ID:
200078077
15.

Cardiac-specific deletion of voltage dependent anion channel 2 leads to dilated cardiomyopathy by altering calcium homeostasis

(Submitter supplied) Voltage dependent anion channel 2 (VDAC2) is an outer mitochondrial membrane porin known to play a significant role in apoptosis and calcium signaling. Abnormalities in calcium homeostasis often leads to electrical and contractile dysfunction and can cause dilated cardiomyopathy and heart failure. However, the specific role of VDAC2 in intracellular calcium dynamics and cardiac function is not well understood. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
9 Samples
Download data: TXT
Series
Accession:
GSE168487
ID:
200168487
16.

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [SOMA-proteomics]

(Submitter supplied) Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remains limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with non-failing or DCM pediatric patient serum activates the fetal gene program (FGP). Here we show that serum treatment with Proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating microRNAs, promote these pathological changes. more...
Organism:
Homo sapiens
Type:
Protein profiling by protein array
Platform:
GPL30452
12 Samples
Download data: TXT
Series
Accession:
GSE181091
ID:
200181091
17.

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Rattus norvegicus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Expression profiling by RT-PCR; Protein profiling by protein array
Platforms:
GPL22396 GPL30452 GPL30448
62 Samples
Download data
Series
Accession:
GSE181051
ID:
200181051
18.

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [Taqman]

(Submitter supplied) Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remains limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with non-failing or DCM pediatric patient serum activates the fetal gene program (FGP). Here we show that serum treatment with Proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating microRNAs, promote these pathological changes. more...
Organism:
Homo sapiens
Type:
Expression profiling by RT-PCR
Platform:
GPL30448
44 Samples
Download data: XLSX
Series
Accession:
GSE181048
ID:
200181048
19.

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [RNA-Seq]

(Submitter supplied) Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remains limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with non-failing or DCM pediatric patient serum activates the fetal gene program (FGP). Here we show that serum treatment with Proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating microRNAs, promote these pathological changes. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL22396
6 Samples
Download data: XLSX
Series
Accession:
GSE181033
ID:
200181033
20.

Deletion of the Lmna Gene in Fibroblasts Causes Senescence-Associated Dilated Cardiomyopathy

(Submitter supplied) Deletion of Lmna in PDGFRA+ cells cause dilated cardiomyoapthy.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
8 Samples
Download data: TXT
Series
Accession:
GSE199078
ID:
200199078
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